From the Department of Preventive Medicine (Carroll, Huffman, Zhao, Liu, Hitsman), Northwestern University Feinberg School of Medicine, Chicago, Illinois; Division of Epidemiology and Community Health (Jacobs), School of Public Health, University of Minnesota, Minneapolis, Minnesota; Department of Psychology (Stewart), Indiana University-Purdue University Indianapolis, Indiana; and Department of Population and Quantitative Health Sciences (Kiefe), University of Massachusetts Medical School, Boston, Massachusetts.
Psychosom Med. 2019 May;81(4):372-379. doi: 10.1097/PSY.0000000000000667.
The aim of the study was to evaluate associations between 15-year trajectories of co-occurring depressive symptoms and smoking with biomarkers of cardiovascular disease at year 15.
In the Coronary Artery Risk Development in Young Adults study, we modeled trajectories of depressive symptoms (Center for Epidemiologic Studies-Depression scale [CES-D]) and smoking (cigarettes per day [CPD]) among 3614 adults followed from year 0 (ages 18-30 years) through year 15 (ages 33-45 years). Biomarkers of inflammation (high-sensitivity C-reactive protein), oxidative stress (superoxide dismutase, F2-isoprostanes), and endothelial dysfunction (soluble intercellular adhesion molecule 1, soluble P-selectin) were assessed at year 15. We conducted separate linear regression analyses with CES-D trajectory, CPD trajectory, and their interaction with each of the five biomarkers.
The sample was 56% women, 47% black, and 40 years old on average at year 15. The CES-D trajectory by CPD trajectory interaction was not associated with any of the biomarkers (all p's > .01). Removing the interaction term, CES-D trajectory was associated with inflammation: higher levels of high-sensitivity C-reactive protein were observed in the subthreshold (β = 0.57, p = .004) and increasing depressive symptoms (β = 1.36, p < .001) trajectories compared with the no depression trajectory. CPD trajectory was associated with oxidative stress and endothelial dysfunction: compared with never smokers, heavy smokers had significantly higher levels of F2-isoprostanes (β = 6.20, p = .001), soluble intercellular adhesion molecule 1 (β = 24.98, p < .001), and soluble P-selectin (β = 2.91, p < .001).
Co-occurring depressive symptoms and smoking do not seem to synergistically convey risk for cardiovascular disease via processes of inflammation, oxidative stress, or endothelial dysfunction. Nonetheless, these results advance our understanding of the complex relationships between modifiable risk factors and chronic disease.
本研究旨在评估 15 年共病抑郁症状和吸烟与 15 年后心血管疾病生物标志物之间的关联。
在“年轻人冠状动脉风险发展研究”中,我们对 3614 名成年人进行了抑郁症状(流行病学研究中心抑郁量表 [CES-D])和吸烟(每天吸烟量 [CPD])轨迹建模,这些成年人从 0 年(18-30 岁)随访到 15 年(33-45 岁)。在 15 年时评估了炎症(高敏 C 反应蛋白)、氧化应激(超氧化物歧化酶、F2-异前列腺素)和内皮功能障碍(可溶性细胞间黏附分子 1、可溶性 P 选择素)的生物标志物。我们对 CES-D 轨迹、CPD 轨迹及其与五个生物标志物中每一个的相互作用进行了单独的线性回归分析。
该样本中 56%为女性,47%为黑人,15 岁时平均年龄为 40 岁。CES-D 轨迹与 CPD 轨迹的相互作用与任何生物标志物均无关(所有 p 值均>.01)。在去除相互作用项后,CES-D 轨迹与炎症有关:与无抑郁轨迹相比,亚阈值(β=0.57,p=.004)和抑郁症状逐渐增加(β=1.36,p<.001)轨迹的高敏 C 反应蛋白水平更高。CPD 轨迹与氧化应激和内皮功能障碍有关:与从不吸烟者相比,重度吸烟者 F2-异前列腺素(β=6.20,p=.001)、可溶性细胞间黏附分子 1(β=24.98,p<.001)和可溶性 P 选择素(β=2.91,p<.001)水平显著更高。
共病抑郁症状和吸烟似乎并没有通过炎症、氧化应激或内皮功能障碍等过程协同传递心血管疾病风险。尽管如此,这些结果还是增进了我们对可改变风险因素与慢性疾病之间复杂关系的理解。